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Not Yet RecruitingNCT06021535

Involvement of the Gut Microbiota in Calcified Aortic Stenosis

Involvement of the Gut Microbiota and Its Metabolites in the Pathophysiology of Calcified Aortic Stenosis

Status
Not Yet Recruiting
Phase
Study type
Observational
Enrollment
100 (estimated)
Sponsor
Insel Gruppe AG, University Hospital Bern · Academic / Other
Sex
All
Age
18 Years – 90 Years
Healthy volunteers
Not accepted

Summary

Calcific aortic stenosis (CAS) is a disease characterized by progressive calcification of the aortic valve, obstructing the passage of blood from the left ventricle into the general circulation. It is the most frequent cause of valve disease in the elderly. To date, no means of preventing the disease has been discovered, and the only treatment available is valve replacement during cardiac surgery, or percutaneous implantation of a valve prosthesis when the narrowing becomes severe and causes symptoms. The intestinal flora or microbiota, the reservoir of all the microorganisms in the gut, is implicated in numerous diseases, particularly of the intestine. But to date, no study has established a link between CAS and microbiota. The intestinal microbiota acts through molecules produced by itself or the host and passing into the bloodstream. In the pathophysiology of CAS, the valve leaflets are breached and do not heal. These molecules can enter and have beneficial or deleterious effects, in particular promoting calcification of aortic valve cells. Concrete objectives: Improve understanding of calcific aortic stenosis in humans Study the composition of intestinal flora in patients with aortic stenosis and compare it with healthy subjects Study the molecules in the intestinal flora likely to be involved in the development of aortic stenosis in humans.

Conditions

Interventions

TypeNameDescription
OTHERNo interventionNo intervention

Timeline

Start date
2024-01-01
Primary completion
2025-12-31
Completion
2028-12-31
First posted
2023-09-01
Last updated
2023-09-01

Source: ClinicalTrials.gov record NCT06021535. Inclusion in this directory is not an endorsement.